Changes in the distribution of extracellular matrix components during neural crest development in Xiphophorus spp. embryos

1994 ◽  
Vol 72 (7) ◽  
pp. 1340-1353 ◽  
Author(s):  
Bahram Sadaghiani ◽  
Bruce J. Crawford ◽  
Juergen R. Vielkind
Keyword(s):  
Extracellular Matrix ◽  
Neural Crest ◽  
Critical Role ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Weak Staining ◽  
Extracellular Matrix Components ◽  
Neural Crest Cell Migration ◽  
And Migration ◽  
Migration Pathways

The changes in distribution of chondroitin sulfate proteoglycans (CSs) and fibronectin (FN), two major components of the extracellular matrix (ECM), are described during the development and migration of neural crest cells in two Xiphophorus species offish, X. helleri (swordtail) and X. maculatus (platyfish), using immunohistochemistry. A detailed description of the developmental changes in HNK-1-positive ECM components is also provided and compared with those of CSs and FN. HNK-1 antigen was also used as a marker for the neural crest cells. Weak staining for CSs, FN, and HNK-1-positive ECM was present in the neural crest cell migration pathways prior to migration of the cells. The level of staining increased dramatically during migration of these cells and decreased again after migration was nearly completed. Staining for CSs was more widespread than staining for FN, while the HNK-1 staining pattern was more clearly restricted to the migratory pathways than those seen with the other two antibodies. The correlation between the spatiotemporal relationship of these ECM components and the segregation and migration of neural crest cells suggests that these ECM molecules may be involved in both initiating and guiding the migration of neural crest cells in these fish. The HNK-1-positive ECM may play a more critical role than CSs and FN.

Signalling between the hindbrain and paraxial tissues dictates neural crest migration pathways

Development ◽  
2002 ◽  
Vol 129 (2) ◽  
pp. 433-442 ◽  
Author(s):  
Paul A. Trainor ◽  
Dorothy Sobieszczuk ◽  
David Wilkinson ◽  
Robb Krumlauf
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Branchial Arches ◽  
Neural Crest Cell Migration ◽  
And Migration ◽  
Migration Pathways ◽  
Crest Cell

Cranial neural crest cells are a pluripotent population of cells derived from the neural tube that migrate into the branchial arches to generate the distinctive bone, connective tissue and peripheral nervous system components characteristic of the vertebrate head. The highly conserved segmental organisation of the vertebrate hindbrain plays an important role in pattering the pathways of neural crest cell migration and in generating the distinct or separate streams of crest cells that form unique structures in each arch. We have used focal injections of DiI into the developing mouse hindbrain in combination with in vitro whole embryo culture to map the patterns of cranial neural crest cell migration into the developing branchial arches. Our results show that mouse hindbrain-derived neural crest cells migrate in three segregated streams adjacent to the even-numbered rhombomeres into the branchial arches, and each stream contains contributions of cells from three rhombomeres in a pattern very similar to that observed in the chick embryo. There are clear neural crest-free zones adjacent to r3 and r5. Furthermore, using grafting and lineage-tracing techniques in cultured mouse embryos to investigate the differential ability of odd and even-numbered segments to generate neural crest cells, we find that odd and even segments have an intrinsic ability to produce equivalent numbers of neural crest cells. This implies that inter-rhombomeric signalling is less important than combinatorial interactions between the hindbrain and the adjacent arch environment in specific regions, in the process of restricting the generation and migration of neural crest cells. This creates crest-free territories and suggests that tissue interactions established during development and patterning of the branchial arches may set up signals that the neural plate is primed to interpret during the progressive events leading to the delamination and migration of neural crest cells. Using interspecies grafting experiments between mouse and chick embryos, we have shown that this process forms part of a conserved mechanism for generating neural crest-free zones and contributing to the separation of migrating crest populations with distinct Hox expression during vertebrate head development.

Evidence for collapsin-1 functioning in the control of neural crest migration in both trunk and hindbrain regions

Development ◽  
1999 ◽  
Vol 126 (10) ◽  
pp. 2181-2189 ◽  
Author(s):  
B.J. Eickholt ◽  
S.L. Mackenzie ◽  
A. Graham ◽  
F.S. Walsh ◽  
P. Doherty
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Axon Growth ◽  
Neural Crest Cells ◽  
Neural Crest Cell Migration ◽  
Neural Crest Migration ◽  
Migration Pathways ◽  
Crest Cell

Collapsin-1 belongs to the Semaphorin family of molecules, several members of which have been implicated in the co-ordination of axon growth and guidance. Collapsin-1 can function as a selective chemorepellent for sensory neurons, however, its early expression within the somites and the cranial neural tube (Shepherd, I., Luo, Y., Raper, J. A. and Chang, S. (1996) Dev. Biol. 173, 185–199) suggest that it might contribute to the control of additional developmental processes in the chick. We now report a detailed study on the expression of collapsin-1 as well as on the distribution of collapsin-1-binding sites in regions where neural crest cell migration occurs. collapsin-1 expression is detected in regions bordering neural crest migration pathways in both the trunk and hindbrain regions and a receptor for collapsin-1, neuropilin-1, is expressed by migrating crest cells derived from both regions. When added to crest cells in vitro, a collapsin-1-Fc chimeric protein induces morphological changes similar to those seen in neuronal growth cones. In order to test the function of collapsin-1 on the migration of neural crest cells, an in vitro assay was used in which collapsin-1-Fc was immobilised in alternating stripes consisting of collapsin-Fc/fibronectin versus fibronectin alone. Explanted neural crest cells derived from both trunk and hindbrain regions avoided the collapsin-Fc-containing substratum. These results suggest that collapsin-1 signalling can contribute to the patterning of neural crest cell migration in the developing chick.

scholarly journals The distribution of tenascin coincides with pathways of neural crest cell migration

Development ◽  
1988 ◽  
Vol 102 (1) ◽  
pp. 237-250 ◽  
Author(s):  
E.J. Mackie ◽  
R.P. Tucker ◽  
W. Halfter ◽  
R. Chiquet-Ehrismann ◽  
H.H. Epperlein
Keyword(s):  
Xenopus Laevis ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Rat Embryos ◽  
The Matrix ◽  
Neural Crest Cell Migration ◽  
Neural Crest Migration ◽  
Migration Pathways

The distribution of the extracellular matrix (ECM) glycoprotein, tenascin, has been compared with that of fibronectin in neural crest migration pathways of Xenopus laevis, quail and rat embryos. In all species studied, the distribution of tenascin, examined by immunohistochemistry, was more closely correlated with pathways of migration than that of fibronectin, which is known to be important for neural crest migration. In Xenopus laevis embryos, anti-tenascin stained the dorsal fin matrix and ECM along the ventral route of migration, but not the ECM found laterally between the ectoderma and somites where neural crest cells do not migrate. In quail embryos, the appearance of tenascin in neural crest pathways was well correlated with the anterior-to-posterior wave of migration. The distribution of tenascin within somites was compared with that of the neural crest marker, HNK-1, in quail embryos. In the dorsal halves of quail somites which contained migrating neural crest cells, the predominant tenascin staining was in the anterior halves of the somites, codistributed with the migrating cells. In rat embryos, tenascin was detectable in the somites only in the anterior halves. Tenascin was not detectable in the matrix of cultured quail neural crest cells, but was in the matrix surrounding somite and notochord cells in vitro. Neural crest cells cultured on a substratum of tenascin did not spread and were rounded. We propose that tenascin is an important factor controlling neural crest morphogenesis, perhaps by modifying the interaction of neural crest cells with fibronectin.

Versican is selectively expressed in embryonic tissues that act as barriers to neural crest cell migration and axon outgrowth

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2303-2312 ◽  
Author(s):  
R.M. Landolt ◽  
L. Vaughan ◽  
K.H. Winterhalter ◽  
D.R. Zimmermann
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Core Protein ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Axon Outgrowth ◽  
Cellular Interactions ◽  
Neural Crest Cell Migration ◽  
Migration Pathways ◽  
Crest Cell

Chondroitin sulfate proteoglycans have been implicated in the regulation of cell migration and pattern formation in the developing peripheral nervous system. To identify whether the large aggregating proteoglycan versican might be mediating these processes, we prepared monospecific antibodies against a recombinant core protein fragment of chick versican. The purified antibodies recognize the predominant versican splice-variants V0 and V1. Using these antibodies, we revealed a close correlation between the spacio-temporal expression of versican and the formation of molecular boundaries flanking or transiently blocking the migration pathways of neural crest cells or motor and sensory axons. Versican is present in the caudal sclerotome, the early dorsolateral tissue underneath the ectoderm, the pelvic girdle precursor and to a certain extent in the perinotochordal mesenchyme. Versican is completely absent from tissues invaded by neural crest cells and extending axons. Upon completion of neural crest cell migration and axon outgrowth, versican expression is shifted to pre-chondrogenic areas. Since versican inhibits cellular interactions with fibronectin, laminin and collagen I in vitro, the selective expression of versican within barrier tissues may be linked to a functional role of versican in the guidance of migratory neural crest cells and outgrowing axons.

Structural and compositional divergencies in the extracellular matrix encountered by neural crest cells in the white mutant axolotl embryo

Development ◽  
1990 ◽  
Vol 109 (3) ◽  
pp. 533-551 ◽  
Author(s):  
R. Perris ◽  
J. Lofberg ◽  
C. Fallstrom ◽  
Y. von Boxberg ◽  
L. Olsson ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Migration ◽  
Neural Crest ◽  
Pigment Cell ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Ruthenium Red ◽  
Neural Crest Cell Migration ◽  
White Mutant ◽  
Crest Cell

The skin of the white mutant axolotl larva is pigmented differently from that of the normal dark due to a local inability of the extracellular matrix (ECM) to support subepidermal migration of neural crest-derived pigment cell precursors. In the present study, we have compared the ECM of neural crest migratory pathways of normal dark and white mutant embryos ultrastructurally, immunohistochemically and biochemically to disclose differences in their structure/composition that could be responsible for the restriction of subepidermal neural crest cell migration in the white mutant axolotl. When examined by electron microscopy, in conjunction with computerized image analysis, the structural assembly of interstitial and basement membrane ECMs of the two embryos was found to be largely comparable. At stages of initial neural crest cell migration, however, fixation of the subepidermal ECM in situ with either Karnovsky-ruthenium red or with periodate-lysine-paraformaldehyde followed by ruthenium red-containing fixatives, revealed that fibrils of the dark matrix were significantly more abundant in associated electron-dense granules. This ultrastructural discrepancy of the white axolotl ECM was specific for the subepidermal region and suggested an abnormal proteoglycan distribution. Dark and white matrices of the medioventral migratory route of neural crest cells had a comparable appearance but differed from the corresponding subepidermal ECMs. Immunohistochemistry revealed only minor differences in the distribution of fibronectin, laminin, collagen types I, and IV, whereas collagen type III appeared differentially distributed in the two embryos. Chondroitin- and chondroitin-6-sulfate-rich proteoglycans were more prevalent in the white mutant embryo than in the dark, especially in the subepidermal space. Membrane microcarriers were utilized to explant site-specifically native ECM for biochemical analysis. Two-dimensional gel electrophoresis of these regional matrices revealed a number of differences in their protein content, principally in constituents of apparent molecular masses of 30–90,000. Taken together our observations suggest that local divergences in the concentration/assembly of low and high molecular mass proteins and proteoglycans of the ECM encountered by the moving neural crest cells account for their disparate migratory behavior in the white mutant axolotl.

Avian neural crest cell migration on laminin: interaction of the alpha1beta1 integrin with distinct laminin-1 domains mediates different adhesive responses

1997 ◽  
Vol 110 (21) ◽  
pp. 2729-2744 ◽  
Author(s):  
N. Desban ◽  
J.L. Duband
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Binding Domains ◽  
Cell Adhesion And Migration ◽  
Neural Crest Cell Migration ◽  
And Migration ◽  
Crest Cell ◽  
Laminin 1

In the present study, to further elucidate the molecular events that control neural crest cell migration, we have analyzed in vitro the adhesive and locomotory response of avian trunk neural crest cells to laminin-1 and searched for the integrin receptors involved in this process. Adhesion of crest cells on laminin-1 was comparable to that found on fibronectin or vitronectin. By contrast, migration was significantly greater on laminin-1 than on the other substrate molecules. Interaction of crest cells with laminin-1 involved two major cell-binding domains situated in different portions of the molecule, namely the E1′ and E8 fragments, which elicited different cellular responses. Cells were poorly spread on the E1′ fragment whereas, on E8, they were extremely flattened and cohesive. Either fragment supported cell locomotion, albeit not as efficiently as laminin-1. Immunoprecipitation and immunocytochemistry analyses revealed that crest cells expressed the alpha1beta1, alpha3beta1, alpha6beta1 and alpha vbeta3 integrins, as well as beta8 integrins, as presumptive laminin-1 receptors, but not alpha6beta4 and alpha2beta1. Immunofluorescence labeling of cultured cells showed that the alpha1, alpha v, beta1 and beta3 subunits were diffuse on the cell surface and in focal contacts. In contrast, alpha3 and beta8 were diffuse, while alpha6 was mostly intracytoplasmic and, secondarily, in focal contacts. Inhibition assays of cell adhesion and migration with function-perturbing antibodies demonstrated that alpha1beta1 played a predominant role in both adhesion and migration on laminin-1 and interacted with either binding sites in the E1′ and E8 fragments. Alpha vbeta3 was also implicated in neural crest cell migration. In contrast, alpha3beta1, alpha6beta1 and the beta8 integrins appeared to play only subsidiary roles in cell adhesion and migration. Finally, the ability of neural crest cells to interact with laminin-1 was found to increase with time in culture, possibly in correlation with changes in alpha3 distribution on the cell surface. In conclusion, our study indicates that (1) the preferential migration of neural crest cells along basal laminae can be accounted for by the ability of laminin-1 to promote migration with great efficiency; (2) interaction with laminin-1 involves two major cell binding domains that are both recognized by the alpha1beta1 integrin; (3) alpha1beta1 integrin can elicit different cellular responses depending on the laminin-1 domains with which it interacts; and (4) changes in the repertoire of integrins expressed by neural crest cells are consistent with the modulations of cell-substratum adhesion occurring throughout migration.

Alternating patterns of cell surface properties and neural crest cell migration during segmentation of the chick hindbrain

Development ◽  
1991 ◽  
Vol 113 (Supplement_2) ◽  
pp. 9-15 ◽  
Author(s):  
Andrew Lumsden ◽  
Sarah Guthrie
Keyword(s):  
Cell Surface ◽  
Neural Crest ◽  
Surface Properties ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Cell Surface Properties ◽  
Branchial Arches ◽  
Neural Crest Cell Migration ◽  
Migration Pathways ◽  
Crest Cell

The developing chick hindbrain is transiently divided into a series of repeating units or rhombomeres. Recent work has shown that an alternating periodicity exists both in the cell surface properties of rhombomeres and in the segmental origin of hindbrain neural crest cells. Experiments in which rhombomeres from different axial levels were confronted in the absence of an interrhombomere boundary showed that odd-numbered segments 3 and 5 combined without generating a boundary, as did even-numbered segments 2, 4 and 6. When rhombomeres originating from adjacent positions, or three rhombomeres distant from one another were combined, a new boundary was regenerated. Mapping of the migration pathways of neural crest cells showed that odd-numbered and even-numbered rhombomeres share properties with respect to the production of neural crest cells. In the hindbrain region the neural crest is segregated into streams. Neural crest cells migrating from rhombomeres 1 and 2, rhombomere 4 and rhombomere 6 respectively populate distinct cranial nerve ganglia and branchial arches. In contrast, rhombomeres 3 and 5 are free of neural crest cells.

The distribution of fibronectin and tenascin along migratory pathways of the neural crest in the trunk of amphibian embryos

Development ◽  
1988 ◽  
Vol 103 (4) ◽  
pp. 743-756 ◽  
Author(s):  
H.H. Epperlein ◽  
W. Halfter ◽  
R.P. Tucker
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Pigment Cells ◽  
Dorsal Fin ◽  
Amphibian Embryos ◽  
Neural Crest Cell Migration ◽  
Crest Cell

It is generally assumed that in amphibian embryos neural crest cells migrate dorsally, where they form the mesenchyme of the dorsal fin, laterally (between somites and epidermis), where they give rise to pigment cells, and ventromedially (between somites and neural tube), where they form the elements of the peripheral nervous system. While there is agreement about the crest migratory routes in the axolotl (Ambystoma mexicanum), different opinions exist about the lateral pathway in Xenopus. We investigated neural crest cell migration in Xenopus (stages 23, 32, 35/36 and 41) using the X. laevis-X. borealis nuclear marker system and could not find evidence for cells migrating laterally. We have also used immunohistochemistry to study the distribution of the extracellular matrix (ECM) glycoproteins fibronectin (FN) and tenascin (TN), which have been implicated in directing neural crest cells during their migrations in avian and mammalian embryos, in the neural crest migratory pathways of Xenopus and the axolotl. In premigratory stages of the crest, both in Xenopus (stage 22) and the axolotl (stage 25), FN was found subepidermally and in extracellular spaces around the neural tube, notochord and somites. The staining was particularly intense in the dorsal part of the embryo, but it was also present along the visceral and parietal layers of the lateral plate mesoderm. TN, in contrast, was found only in the anterior trunk mesoderm in Xenopus; in the axolotl, it was absent. During neural crest cell migration in Xenopus (stages 25–33) and the axolotl (stages 28–35), anti-FN stained the ECM throughout the embryo, whereas anti-TN staining was limited to dorsal regions. There it was particularly intense medially, i.e. in the dorsal fin, around the neural tube, notochord, dorsal aorta and at the medial surface of the somites (stage 35 in both species). During postmigratory stages in Xenopus (stage 40), anti-FN staining was less intense than anti-TN staining. In culture, axolotl neural crest cells spread differently on FN- and TN-coated substrata. On TN, the onset of cellular outgrowth was delayed for about 1 day, but after 3 days the extent of outgrowth was indistinguishable from cultures grown on FN. However, neural crest cells in 3-day-old cultures were much more flattened on FN than on TN. We conclude that both FN and TN are present in the ECM that lines the neural crest migratory pathways of amphibian embryos at the time when the neural crest cells are actively migrating. FN is present in the embryonic ECM before the onset of neural crest migration.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Neural crest cell migration: requirements for exogenous fibronectin and high cell density.

1983 ◽  
Vol 96 (2) ◽  
pp. 462-473 ◽  
Author(s):  
R A Rovasio ◽  
A Delouvee ◽  
K M Yamada ◽  
R Timpl ◽  
J P Thiery
Keyword(s):  
Cell Adhesion ◽  
Neural Crest ◽  
Type I Collagen ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Type I ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Crest Cell

Cells of the neural crest participate in a major class of cell migratory events during embryonic development. From indirect evidence, it has been suggested that fibronectin (FN) might be involved in these events. We have directly tested the role of FN in neural crest cell adhesion and migration using several in vitro model systems. Avian trunk neural crest cells adhered readily to purified plasma FN substrates and to extracellular matrices containing cellular FN. Their adhesion was inhibited by antibodies to a cell-binding fragment of FN. In contrast, these cells did not adhere to glass, type I collagen, or to bovine serum albumin in the absence of FN. Neural crest cell adhesion to laminin (LN) was significantly less than to FN; however, culturing of crest cells under conditions producing an epithelioid phenotype resulted in cells that could bind equally as well to LN as to FN. The migration of neural crest cells appeared to depend on both the substrate and the extent of cell interactions. Cells migrated substantially more rapidly on FN than on LN or type I collagen substrates; if provided a choice between stripes of FN and glass or LN, cells migrated preferentially on the FN. Migration was inhibited by antibodies against the cell-binding region of FN, and the inhibition could be reversed by a subsequent addition of exogenous FN. However, the migration on FN was random and displayed little persistence of direction unless cells were at high densities that permitted frequent contacts. The in vitro rate of migration of cells on FN-containing matrices was 50 microns/h, similar to their migration rates along the narrow regions of FN-containing extracellular matrix in migratory pathways in vivo. These results indicate that FN is important for neural crest cell adhesion and migration and that the high cell densities of neural crest cells in the transient, narrow migratory pathways found in the embryo are necessary for effective directional migration.

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